There are presently a number of methods and techniques for the treatment of cancer, among which may be included: radiation therapy, chemotherapy, immunotherapy, and surgery. The common characteristic for all of these techniques as well as any other presently known technique is that they are extracellular in scope; that is, the cancer cell is attacked and attempted to be killed through application of the killing force or medium outside of the cell; the only known exception being, U.S. Pat. No. 4,106,488, Cancer Treatment Method, Robert Thomas Gordon, issued Aug. 15, 1978, of which this invention is an extension of the technology therein described.
The extracellular approach is found to be less effective because of the difficulties of penetrating the outer membrane of the cancer cell that is composed of two protein layers with a lipid layer in between. Of even greater significance is that in order to overcome the protection afforded the cell by the cell membrane in any extracellular techniques, the attack on the cancer cells must be of such intensity that considerable damage is caused to the normal cells resulting in severe side effects upon the subject. These side effects have been found to limit considerably the effectiveness and usefulness of these extracellular treatments.
A safe and effective cancer treatment has been the goal of investigators for a substantial period of time. Such a technique to be successful in the destruction of the cancer cells must be selective in effect upon the cancer cells and produce no irreversible damage to the normal cells. In sum, cancer treatment must selectively differentiate cancer cells from normal cells and must selectively weaken or kill the cancer cells without affecting the normal cells.
It has been known that there are certain physical differences that exist between cancer cells and normal cells. One primary physical difference that exists is the temperature differential characteristics between the cancer cells and the normal cells. Cancer cells, because of their higher rates of metabolism, have higher resting temperatures compared to normal cells. In the living cell, the normal temperature of the cancer cell is known to be 37.5.degree. Centigrade, while that of the normal cell is 37.degree. Centigrade. Another physical characteristic that differentiates the cancer cells from the normal cells is that cancer cells die at lower temperatures than do normal cells. The temperature at which a normal cell will be killed and thereby irreversibly will be unable to perform normal cell functions is a temperature of 46.5.degree. Centigrade, on the average. The cancer cell, in contrast, will be killed at the lower temperature of 45.5.degree. Centigrade. The temperature elevation increment necessary to cause death in the cancer cell is determined to be at least approximately 8.0.degree. Centigrade, while the normal cell can withstand a temperature increase of at least 9.5.degree. Centigrade.
It is known, therefore, that with a given precisely controlled increment of heat, the cancer cells can be selectively destroyed without injury to the normal cells. On the basis of this known differential in temperature characteristics, a number of extracellular attempts have been made to treat cancer by heating the cancer cells in the body. This concept of treatment is referred to as hyperthermia. To achieve these higher temperatures in the cancer cells, researchers have attempted a number of methods including inducing high fevers, utilizing hot baths, diathermy, applying hot wax, and even the implantation of various heating devices in the area of the cancer.
Presently, none of the various known approaches to treat cancer have been truly effective and all have the common characteristic of approaching the problem by treating the cancer cell extracellularly; the only known exception being, U.S. Pat. No. 4,106,488, Cancer Treatment Method, Dr. Robert Thomas Gordon, issued Aug. 15, 1978. The outer membrane of the cancer cell being composed of lipids and proteins, is a poor thermal conductor, thus making it difficult for the application of heat by external means to penetrate into the interior of the cell where the intracellular temperature must be raised to effect the death of the cell. If, through the extracellular approaches of the prior hyperthermia techniques, the temperatures were raised sufficiently to effect an adequate intracellular temperature to kill the cancer cells, many of the normal cells adjacent the application of heat would be destroyed as well.
It has been known that the nuclei of cancer cells and the nuclei of normal cells possess some differences. The alterations which occur in a cell to produce malignancy either take place in, or are transmitted to, the nucleus. This is evident by the fact that the cells produced by tumor cell multiplication possess the same characteristics as the original tumor cell.
A large amount of work has been done "in vitro" concerning the magnetic resonant frequencies of cancer tissues as compared to those of normal tissues. Differences have been attributed to differences in the amount of water present in the cancer cells and the way in which the water molecules are ordered. A key to this process lies in the nuclear differences, including energy changes characteristic of structural and conformational changes in the deoxyribonucleic acid and the histones of the nucleus, including their relationship, resulting in differential resonant frequencies for the cancer cells from the normal cells.
A further key to this process is the additional changes in intracellular biophysical characteristics which occur in this process. Included in these changes is the intracellular production of interferon and/or prostaglandins. The production of interferon in the past has been shown to be triggered by foreign agents or materials which alter the internal biophysical characteristics of the cell by increases in the intracellular temperature or energy levels.
Due to the unstable characteristics of interferon and prostaglandins, even if interferon and prostaglandins were to be synthesized and subsequently injected intravascularly into a subject, the effectiveness of the synthesized interferon and/or prostaglandins would be limited due to the loss of time between injection into the subject and the time when the synthesized interferon and/or prostaglandins would reach the cellular level where their effectiveness is required. Interferon and prostaglandins are most effective when their production is stimulated intracellularly so that their peak effectiveness and potential are utilized, where required, intracellularly.